Introduction

BACKGROUND:
Previous population based studies including both the Global allergy & Asthma European (GA2LEN) survey1 and Canadian National Population Health survey2 suggest a strong association between CRS prevalence and active smoking, with a possible dose dependent association in the GA2LEN1 study finding a 1.5% increase in prevalence for each year smoked. Several national and international studies have also looked at smoking and its relationship to chronic rhinosinusitis (CRS); with eleven out of thirteen studies in a recent systematic review reporting increased CRS prevalence in smokers.3 Conversely a small number of studies4,5 have reported a lack of any strong association and some previous epidemiological studies have the potential to overestimate disease prevalence on methodological design. The 2000 National (England and Wales) Sino-Nasal Audit identified that around 20% of patients with CRS/ nasal polyps regarded themselves as active smokers, compared to a national adult smoking rate at the time of 27%.6
A number of studies have examined the possible effects of smoking on the sinonasal mucosa with variable results. This lack of consensus may result from a lack of standardisation but also highlights that a combination of different pathophysiological mechanisms may co-exist. Chistenson et al3 summarised prominent findings from available invitro and invivo studies. In vitro studies have suggested a number of possible mechanisms with smoking causing alterations in chloride ion transport,7, 8 reduced mucociliary clearance8 and or reduced ciliary generation.9 In vivo results are also conflicting with possible changes in histology,10 mucociliary transport11 and inflammatory cytokines12 underlying disease development. The aetiological role of the sinonasal microbiome is another topical area where there has been increasing research with respect to smoking and its potential roles in altering this microbiome and or encouraging biofilm formation.13Some in vitro experiments have shown that repetitive exposure of tobacco smoke can promote biofilm formation within bacterial isolates from CRS patients,14however any underlying mechanism remains poorly understood. In contrast Zhang et al15 failed to find any difference between smoking status and biofilm formation within sinus cultures taken at the time of endoscopic surgery.
With such heterogeneity in existing research no strong conclusions can currently be drawn on the exact pathophysiological mechanisms involved in CRS. Understanding the relationship of smoking to the health of sinonasal mucosa is however an important step to help direct patient care and education and may allow more accurate discussion on the likely clinical outcomes of any subsequent therapy and surgical intervention.
The Chronic Rhinosinusitis Epidemiology Study (CRES) was a prospective, questionnaire-based, case-control study conducted between October 2007 and September 2013 at thirty tertiary/secondary care sites across the United Kingdom. Patients with diagnosed CRS alongside healthy control subjects were asked to complete a single, study-specific questionnaire, capturing a variety of demographic and socio-economic variables, environmental exposures and medical co-morbidities (See appendix 1).
CRES was designed to distinguish differences in socio-economic status, geography, medical/psychiatric co-morbidity, lifestyle and overall quality of life between patients with CRS and healthy controls. The specific aim of this analysis of the CRES database was to determine whether active smoking represents a risk factor for CRS development and/ or whether smokers experience an increased symptom burden than non-smokers. Understanding causal links will allow for more informed decision making and may clarify the potential role of smoking cessation in CRS symptom control.